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  • 1
    Electronic Resource
    Electronic Resource
    Adhesion of colorectal carcinoma cells to the endothelium is mediated by cytokines from CEA stimulated Kupffer cells (1998)
    Springer
    Clinical & experimental metastasis 16 (1998), S. 703-712 
    Details
    ISSN: 1573-7276
    Keywords: Kupffer cells ; CEA-binding 80 kDa protein ; proinflammatory cytokines ; endothelial cells ; adhesion molecules ; metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We hypothesize that a major factor regulating hepatic metastasis is the ability of CEA (carcinoembryonic antigen) producing colorectal carcinomas to activate Kupffer cells. CEA and NCA (nonspecific cross-reacting antigen) bind to an 80 kDa Kupffer cell receptor by the peptide sequence PELPK and stimulate cytokine production. Cytokines induce sinusoidal endothelial cells to express intercellular adhesion molecules and increase adhesion of the tumor cells and retention in the liver. In this study human Kupffer cells were acti-vated in vitro with CEA, NCA, and the peptide PELPK. This resulted in release of IL-1b, TNF-a and IL-6. CEA non-producing MIP-101 colon carcinoma cells labeled with 51 Cr were incubated on monolayers of ECV-304 human umbilical vein endothelial cells treated with these Kupffer cell derived cytokines or with comparable recombinant human (rH) cytokines. Specific antibodies to the adhesion molecules ICAM-1, VCAM-1, E-selectin and b 2 integrin were used to block their functions. A significant enhancement in the adhesion of colorectal carcinoma cells occurred when endothelial cells were stimulated with a very low concentration of Kupffer-cell derived cytokines. Activated endothelium demonstrated significant up-regu-lation primarily of ICAM-1. The adhesion was blocked by an antibody to ICAM-1. A combination of Kupffer-cell derived cytokines was more effective than IL-1b or TNF-a alone. IL-6 alone did not influence adhesion under our conditions. Our results suggest a mechanism for CEA in the modulation of colorectal carcinoma adhesion to the hepatic endothelium and its enhancement of metastatic potential.© Kluwer Academic Publishers 1998
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006576627429
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  • 2
    Electronic Resource
    Electronic Resource
    Human and murine Kupffer cell function may be altered by both intrahepatic and intrasplenic tumor deposits (1993)
    Springer
    Clinical & experimental metastasis 11 (1993), S. 175-182 
    Details
    ISSN: 1573-7276
    Keywords: hepatic metastases ; Kupffer cells ; splenic metastases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: The liver is the most common site of hematogenous metastases from colorectal carcinoma. Kupffer cells (KC), which line the hepatic sinusoids, may form the first line of defense against circulating tumor cells. The purpose of this study was to determine the effect of hepatic metastases and intro-abdominal tumor growth on KC binding of human colorectal carcinoma (HCRC) cells. MIP-101, a poorly metastatic cell line, and CX-1, a highly metastatic cell line, were injected intrasplenically into nude mice and KC were isolated by collagenase perfusion at varying intervals after injection. Conditioned media were collected from MIP-101, CCL 188 and CX-1 to determine their in vitro effect on KC function. KC from MIP-101 injected mice (14% liver metastases, 100% splenic tumors) bound a significantly greater number of MIP-101 and clone A cells than CX-1 cells in vitro. KC isolated from mice 5 weeks after CX-1 injection (100% liver metastases) also showed increased binding of MIP-101 and clone A cells compared to CX-1 cells. Similar results were obtained when tumor cell binding to normal human liver KC was compared to binding to KC from human livers from patients with hepatic metastasis from colorectal cancer. In contrast KC obtained from mice 3 weeks after CX-1 injection (44% liver metastases) showed significantly decreased binding of MIP-101 and clone A cells. The conditioned medium from CX-1 cells significantly decreased the in vitro binding of both MIP-101 and CX-1 by KC. These results indicate that the ability of KC to bind HCRC cells (which precedes phagocytosis and tumor cell killing) is a dynamic function and affected by concomitant tumor growth. HCRC cells may alter KC function via the production of specific tumor-derived soluble factors. In order to devise new and more effective therapeutic options in the treatment of liver metastases the nature of this tumor cell-KC interaction must be better understood.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00114975
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  • 3
    Electronic Resource
    Electronic Resource
    Hepatic clearance and metabolism in the rat of a human breast cancer associated glycoprotein (GCDFP-15) (1988)
    Springer
    Breast cancer research and treatment 12 (1988), S. 235-243 
    Details
    ISSN: 1573-7217
    Keywords: clearance ; cystic disease fluid protein ; fibrinogen ; GCDFP-15 ; glycoprotein ; Kupffer cells ; immunocytochemistry ; metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Gross Cystic Disease Fluid Protein (GCDFP-15) is a 60,000 dalton glycoprotein isolated from human breast cyst fluid, composed of four 15,000 dalton monomers. Carbohydrate analysis indicates that each monomer has a single carbohydrate chain of the complex type. GCDFP-15 intravenously injected into rats showed a rapid circulatory clearance, the rate of clearance being faster in female animals [t1/2 = 12.8 (± 2.0) min. females, and 16.7 (± 2.6) min. males]. The major organs of clearance were the liver (70%) and kidneys (15%). Immunoperoxidase staining showed localization in Kupffer cells and the proximal convoluted tubules of the kidney. Removal of sialic acid from GCDFP-15 resulted in a more rapid clearance (t1/2 = 2.2 min) by the liver (85%). This clearance was inhibited by coinjection of asialo alpha1 acid glycoprotein. About 3% of GCDFP-15 was excreted in bile with a transit time through the liver of 38 min. Examination of the uptake of GCDFP-15 by isolated rat Kupffer cells showed that yeast mannan, fucosylated BSA, and carcinoembryonic antigen (CEA) failed to inhibit uptake, though the binding of GCDFP-15 was clearly saturable. This suggests that a novel receptor system on the rat Kupffer cell may be responsible for GCDFP-15 clearance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01805944
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  • 4
    Electronic Resource
    Electronic Resource
    Serum β-N-acetyl hexosaminidase and bile acid levels in patients with benign and malignant biliary obstruction (1988)
    Springer
    Digestive diseases and sciences 33 (1988), S. 189-192 
    Details
    ISSN: 1573-2568
    Keywords: β-N-acetyl hexosaminidase ; Kupffer cells ; benign and malignant biliary obstruction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract β-N-Acetyl hexosaminidase (β-NAH), a lysosomal enzyme, was measured in the plasma of 15 patients with malignant extrahepatic biliary obstruction, 14 with benign extrahepatic obstruction, and 15 with long- standing benign intrahepatic cholestasis. β-NAH was correlated with total serum bile acid levels. The correlation was significant (P〈0.05) for the malignant and benign intrahepatic obstructions but not for the benign extrahepatic obstructions. This is consistent with the idea that circulating high levels of bile acids in patients with long-standing biliary obstruction may cause damage to Kupffer cell membranes and to their receptors for β-N-acetyl hexosaminidase, impeding the clearance of the enzyme from the circulation resulting in elevated serum levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01535732
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